This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Objective: To determine fetal, neonatal and adult markers reflecting mechanism of fetal programming of polycystic ovary syndrome (PCOS). This project continues to determine fetal and neonatal consequences of exposing female rhesus monkey fetuses to androgen excess during early gestation. Current results indicate that a hyperglycemic pregnancy induced by the androgen excess given to pregnant rhesus mothers may contribute to altered morphology of pancreatic islets in exposed female infants that may explain functional alterations in insulin-mediated regulation of glucose. This work provides additional direct evidence for fetal programming of metabolic defects in this nonhuman primate model of PCOS. This research used WNPRC Assay Services, Pathology Services and Animal Services. PUBLICATIONS: Abbott DH, Dumesic DA. 2009. Adult polycystic ovary. Highlights 17:13-18. Abbott DH, Tarantal AF, Dumesic DA. 2009 Fetal, infant, adolescent and adult phenotypes of polycystic ovary syndrome in prenatally androgenized female rhesus monkeys. Am J Primatol. 71:776-784. Dumesic DA, Patankar M, Barnett DK, Lesnick TG, Hutcherson BA, Abbott DH. 2009 Early prenatal androgenization results in diminished ovarian reserve in adult female rhesus monkeys. Hum Reprod. 24:3188-3195.